Shanghai Jiaotong Daxue xuebao. Yixue ban (Mar 2024)

Research progress in pathophysiological and molecular mechanism changes during decompensated phase of portal hypertension in liver cirrhosis

  • FAN Qiang,
  • WU Guangbo,
  • ZHAO Jinbo,
  • ZHENG Lei,
  • LUO Meng

DOI
https://doi.org/10.3969/j.issn.1674-8115.2024.03.011
Journal volume & issue
Vol. 44, no. 3
pp. 379 – 384

Abstract

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Cirrhosis caused by multiple etiologies can lead to portal hypertension. The prognosis of patients with portal hypertension in decompensated cirrhosis is significantly poor. Disorders in the patient′s internal environment caused by various complications often evolve into organ failure both inside and outside the liver. For cirrhosis caused by different etiologies, there are still some relief drugs used in the early stages, but the mechanism of disease progression in patients with decompensated cirrhosis and portal hypertension is currently unclear, and there is a lack of effective treatment plans for disease progression. Therefore, revealing the pathophysiological mechanisms of decompensated cirrhosis with portal hypertension and seeking effective drug targets for treating this disease have become the focus of current research. This article summarizes the pathological and physiological changes of intrahepatic and extrahepatic organ failure during the decompensated phase of liver cirrhosis, and briefly describes the cellular and molecular regulatory mechanisms related to intrahepatic vascular resistance, portal system, cardiovascular system, and inflammatory mediators. By comprehensively analyzing the pathological and physiological development process of decompensated cirrhosis with portal hypertension, the potential cellular and molecular mechanisms that cause disease deterioration or remission can be better understood, which can help improve the accuracy of disease diagnosis and the correct grasp of disease staging. In addition, identifying drug treatment targets to block the progression of the disease will guide clinical staff to better cope with refractory portal hypertension, and even improve the prognosis of patients.

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